摘要:

This study was carried out to assess the diagnostic accuracy of a new gastrointestinal cancer antigen (GICA) defined by a monoclonal antibody. Its sensitivity and specificity were assayed in a group of patients with different pancreatic diseases (10 acute pancreatitis, 27 chronic pancreatitis, 22 cancers of the pancreas) and in 29 normal individuals. The concentration of GICA was always inferior to 37 units/ml (our discriminant limit between cancer and noncancer patients) both in cases with chronic pancreatitis and in healthy subjects. Increased levels of the antigen were found in 16/22 (72.7%) pancreatic cancer patients and in 3/10 (33.3%) cases with acute pancreatitis. The assay was within the normal range in 2 (28.6%) out of 7 cancers judged resectable. The test is simple and rapid, but its relative sensitivity and the frequent elevation of GICA in other adenocarcinomas of the gastrointestinal tract make it unsuitable for screening programs in pancreatic cancer. Even its use for early diagnosis of cancer of the pancreas does not seem promising. The major finding of our study is the lack of false-positives in patients with chronic pancreatitis and therefore the usefulness of this test in differentiating preoperatively between chronic inflammation and cancer of the gland. Frequent increase of the marker in patients with acute pancreatitis is not yet clear.

ISSN:0012-2823    

DOI:10.1159/000199000

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The present experiment demonstrated that relatively high doses of acetazolamide (100 and 200 mg/kg s.c.) induced severe gastric hemorrhagic ulceration in rats. This ulceration was aggravated by oral administration of HC1, but was inhibited by NaHCCO3. Further, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were affirmed by an increase in serotonin and histamine released from the stomach after acetazolamide treatment. Acetazolamide injection also increased the protein level, but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increases in serotonin and histamine released may also have been contributing factors for gastric ulcer formation.

ISSN:0012-2823    

DOI:10.1159/000199001

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The effects of omeprazole, a substituted benzimidazole, on gastric acid secretion and on right atrial beating frequency have been investigated in guinea pig preparations in vitro. Cimetidine was used as a reference compound. Omeprazole, at 10-6mol/l, inhibited basal acid secretion, whereas cimetidine, at 10-5 mol/l, did not. There were also differences in the effects on stimulated secretion. Cimetidine (10-5 mol/l) competitively inhibited histamine-stimulated acid secretion without affecting the maximal histamine response. In contrast, omeprazole concentration dependently depressed (EC50 ∼ 5 × 10-7 mol/l) the maximal histamine response without any effect on the histamine sensitivity. Furthermore, dibutyryl-cAMP-stimulated acid secretion was inhibited by omeprazole but not by cimetidine. The inhibitory effect of omeprazole (2 × 10-6 mol/l) on histamine-stimulated acid secretion was reversed by repeated washing of the serosal side of the mucosa. Omeprazole was devoid of histamine H2 receptor antagonistic activity, since it had no effect on the chronotropic response to histamine in the guinea pig right atrium. It is concluded that omeprazole inhibits gastric acid secretion by a non-histaminergic, reversible mechanism and that the site of action is beyond the cAMP step within the parietal c

ISSN:0012-2823    

DOI:10.1159/000199002

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The present study was undertaken to determine whether atropine inhibits the plasma cholecystokinin (CCK) response to intraduodenal fat. Plasma CCK concentrations were measured by radioimmunoassay using two sequence-specific antibodies. Antibody 1703 bound to all COOH-terminal CCK peptides containing at least 14 amino acid residues, while antibody T204 was specific for the sulphated tyrosine region of CCK. Intraduodenal instillation of 60 ml corn oil in 6 normal subjects induced significant increases in plasma CCK. Intravenous administration of atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg · h over 3 h) resulted in significant inhibition of plasma CCK concentrations at 10, 20 and 30 min (antibody 1703) and at 20 and 30 min (antibody T204) after instillation of fat. However, the peak increments in plasma CCK during atropine (8.6 ± 1.9 pmol/l, antibody 1703; 5.4 ± 1.1 pmol/l, antibody T204) were not different from those found without atropine (6.3 ± 0.8 pmol/l, antibody 1703; 3.9 ± 0.9 pmol/l, antibody T204). Similarly, the integrated plasma CCK secretion after intraduodenal fat was not significantly different when measured during atropine (461 ± 119 pmol/l·3 h, antibody 1703; 269 ± 97 pmol/l·3 h, antibody T204) and without atropine (428 ± 62 pmol/l·3 h, antibody 1703; 188 ± 66 pmol/l·3 h).It is concluded that administration of atropine delays but does not inhibit the CCK response to intraduodenal cor

ISSN:0012-2823    

DOI:10.1159/000199003

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

In this study we have performed a quantitative analysis of antral gastrin cells in 9 uraemic patients under dialytic treatment compared to a group of 10 chronic gastritis patients with a similar histological degree of gastritis. Immunocytochemistry was carried out on endoscopic biopsies of both groups. Using a computerised image analysing system we showed a significant increase of G-cell density (number of cells/mm2) in uraemic patients compared to non-uraemics (p < 0.001). These findings provide a further morphological basis for the elevation of gastrin levels in chronic uraemic patients, suggesting the existence of a specific factor inducing G-cell proliferation in these patients.

ISSN:0012-2823    

DOI:10.1159/000199004

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Cancer cells in culture, and their corresponding nude mouse transplantable tumors, derived from azaserine-induced rat pancreatic acinar cell carcinomas showed a shift from high to low molecular weight glycoproteins when compared with normal, fetal, and regenerating pancreas. A 51,000-dalton glycoprotein was present only in the transplantable nude mouse tumors. Cancer cells and transplantable tumors showed elevated levels of glycosidases, and the former showed higher activities than the latter. Some of the glycosidase activities in host pancreas and liver were elevated.

ISSN:0012-2823    

DOI:10.1159/000199005

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Germ-free and conventional rats were fed a semi-synthetic diet including 10% wheat bran for 1 month. They were compared to similar rats fed the same diet without bran. Transit of polyethylene glycol (PEG) 4000 was studied in giving the marker either in saline or in the diet. The presence of a bacterial flora was found to accelerate small intestine transit and total transit. The ingestion of solid food slowed gastric emptying but had little effect on small intestine transit. Wheat bran slowed gastric emptying of PEG in most of the experimental groups. It had no significant effect on small intestine transit except in germ-free rats having received the marker in solid food. It accelerated total transit in germ-free and conventional rats. The results suggest that bran mainly exerts its action in the hindgut. The role of microflora in this action of bran is discussed.

ISSN:0012-2823    

DOI:10.1159/000199006

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The one-day NBT-PABA/14C-PABA has been performed on 58 consecutive subjects with suspected or established pancreatic disease. 23 of these were normal subjects, 12 were subsequently shown to have other gastrointestinal disease and 23 had proven pancreatic disease. A PABA excretion index (PEI) has been calculated and, using our lower limit of normality (0.61), the test has shown an overall sensitivity of 83 % and specificity of 89 %. False positives were a particular problem in the other gastrointestinal disease group (25%). There was a close correlation between PEI and Lundh mean tryptic activity (r = 0.89). These results indicate that this test is a satisfactory screening test for pancreatic exocrine disease and is easier to perform with less likelihood of error than many other non-invasive tests of pancreatic function.

ISSN:0012-2823    

DOI:10.1159/000199007

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

An experimental model of massive small bowel resection and colonic autograft in an antiperistaltic fashion in between the remnants of jejunum and ileum was developed in Rhesus monkeys. The gross morphological changes showed significant (p < 0.001) lengthening and dilatation of the remnant jejunum, ileum and the colonic graft. Hypertrophy and hyperplasia of the mucosal and muscular layers of all the 3 segments was revealed by morphometric studies and the estimation of the nucleic acid content of the mucosa. All the 3 segments of the bowel showed a significant increase (p < 0.001) in the uptake of D-glucose, L-alanine and L-phenylalanine when compared to the control animals. These changes were more pronounced in the animals kept for longer duration. Phlorizin was found to be inhibitory for the uptake of D-glucose in the grafted colon, suggesting the induction of an active nonelectrolyte transport process in the autografted colon. The present study suggests that the colonic loop adapts itself to the functions of the small bowel along with the compensatory adaptation of the remnant jejunum and the ileum for the loss of absorptive surface secondary to massive small bowel resection.

ISSN:0012-2823    

DOI:10.1159/000199008

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Lysophospholipase (EC 3.1.1.5) and phospholipase A2 (EC 3.1.1.4) were determined in ileal mucosa from patients with Crohn’s disease (CD) and non-inflammatory bowel diseases (NIBD). In addition, the activities of alkaline phosphatase, sucrase, maltase, and lactase were determined. The lysophospholipase activity, like that of alkaline phosphatase, sucrase and maltase, was decreased in affected areas of CD, whereas the phospholipase A2 activity was rather increased. Lysophospholipase and phospholipase A2 activities in apparently unaffected mucosa from CD patients were in between those in healthy mucosa from NIBD patients and those in affected mucosa from CD patients. These findings point to the possibility that the mucosal activity of lysophospholipase, like that of other brush border enzymes, is decreased in CD. This may render the mucosa less capable to handle lysolecithin, a potentially harmful agent formed in the intestine and known to induce inflammation in a number of experimental system

ISSN:0012-2823    

DOI:10.1159/000199009

出版商:S. Karger AG    

年代:1984

数据来源: Karger